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目的:探讨氯化锂对脓毒症大鼠的促炎细胞因子及氧化损伤的影响。方法:将50只Wistar大鼠按随机数字表随机分为假手术组(S组,n=10)、模型组(CLP组,n=20)、氯化锂干预组(CLP+Li Cl组,n=20),每组又分为8 h、16 h、24 h 3个时间观察点亚组,CLP组采用盲肠结扎穿孔术(CLP)制备脓毒症模型。氯化锂干预组于CLP手术后立即给予腹腔注射Li Cl溶液(50 mg/Kg),假手术组和CLP组给予等量生理盐水腹腔注射。每组每只大鼠分别于术后8 h、16 h、24 h采集眼眶静脉血检测其中肿瘤坏死因子α(TNF-α)、白介素6(IL-6)、超氧化物歧化酶(SOD)、丙二醛(MDA)浓度,并记录术后24 h各组大鼠生存率。结果:与S组相比,CLP组及CLP+Li Cl组各时间点血清TNF-α、IL-6和MDA的浓度上升,SOD浓度降低,差异有统计学意义(P<0.05);与CLP组同时间点比较,CLP+Li Cl组血清TNF-α、IL-6和MDA的浓度下降,SOD浓度升高;与CLP组术后24h生存率相比,CLP+Li Cl组生存率提高,差异有统计学意义(P<0.05)。结论:氯化锂可能通过抑制炎性细胞因子释放以及减轻氧化应激损伤的机制实现提高脓毒症大鼠生存率的作用。
Objective: To investigate the effects of lithium chloride on pro-inflammatory cytokines and oxidative damage in septic rats. Methods: Fifty Wistar rats were randomly divided into sham operation group (S group, n = 10), model group (CLP group, n = 20), lithium chloride intervention group n = 20). The rats in each group were divided into 3 sub-groups: 8 h, 16 h, and 24 h. The CLP group was used CLP to prepare sepsis model. LiCl solution (50 mg / Kg) was injected intraperitoneally in lithium chloride intervention group immediately after CLP operation. The rats in sham operation group and CLP group were given intraperitoneal injection of normal saline. The orbital venous blood was collected at 8 h, 16 h and 24 h after operation in each group to detect the levels of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and superoxide dismutase (SOD) , Malondialdehyde (MDA) concentration, and the survival rate of rats in each group was recorded 24 h after operation. Results: Compared with S group, the concentrations of serum TNF-α, IL-6 and MDA in CLP group and CLP + LiCl group increased at each time point and the concentration of SOD decreased (P <0.05) In the CLP + Li Cl group, the concentrations of TNF-α, IL-6 and MDA were decreased and the SOD concentration was increased in the CLP + Li Cl group. Compared with the CLP group, the survival rate of CLP + The difference was statistically significant (P <0.05). Conclusion: Lithium chloride can improve the survival rate of septic rats by inhibiting the release of inflammatory cytokines and alleviating the mechanism of oxidative stress injury.